PT1015 Lesson 1_ Introduction and Generalities PDF

LESSON 1: INTRODUCTION AND GENERALITIES 2ND SEMESTER |A.Y. 2024-2025|PROF. TRANSCRIBED BY: MAVI LAUDICO -​ Production of new cells in the blood because inside...

LESSON 1: INTRODUCTION AND GENERALITIES 2ND SEMESTER |A.Y. 2024-2025|PROF. TRANSCRIBED BY: MAVI LAUDICO -​ Production of new cells in the blood because inside the bone it has red marrow, inside red marrow contains stem cells that produces the new blood Orthopedics cells 6. Mineral storage and release ​ Deals with disorders of musculoskeletal system -​ Particularly calcium phosphorus for muscles and ​ Second to cardiovascular disease in frequency nerves ​ Second most common cause of visits to 7. Fat storage in yellow marrow physicians 8. Acid base (pH) balance ​ Orthos - straight -​ Because our bones releases alkaline that helps in ​ Pais - child the balance ○​ Initially used for children 9. Stores and periodically release growth factors ​ Emphasis on prevention and correction of 10. Detoxification deformity and disability -​ If there is anything toxic in the bone, there is a cell ​ Covers conditions that affect the musculoskeletal on the bone that eats it up ○​ Includes joints, ligaments, and muscles Scope of Orthopedics Cortical vs. Cancellous Bone ​ Injuries Types of bony tissues: ​ Diseases -​ Cortical bone and Cancellous bone ​ Deformities ​ —of bones and joints and related structures such as ​ Cortical (compact) bone muscles, tendons, ligaments and nerve ○​ Constitutes 80% of the skeleton ○​ Usually found outside of the bone and on Orthopedic Surgery the shafts ○​ Consists of tightly packed osteons or ​ Medical specialty that includes the investigation, haversian systems preservation, and restoration of the form and ​ Connected by Haversian or function of the extremities, spine and associated Volkmann’s canals structures by medical, surgical and physical ​ Contains arterioles, venules, methods capillaries, nerves, lymphatic ​ Orthopedic surgeons do surgery, but rehab doctors channels don’t ​ In one osteon contains central canal where the blood supply, nerves, and lymphatics are Bone connected ​ Cancellous bone ​ Highly vascular form of connective tissue ○​ Spongy type ​ Collagen, calcium phosphate, water, amorphous ○​ Found within proteins, and cells ○​ Consists 40% of bones ​ Most rigid of the connective tissue ​ Dynamic tissue that undergoes constant Cortical (compact) Bone metabolism and remodeling ○​ Your bone is constantly changing same as ​ Interstitial lamellae: between osteons your cells ○​ Fibrils connect lamellae but do not cross ○​ Every bone differs in time of remodeling; it cement lines does not happen all at once; it will take ○​ Cement line define the outer border of an approximately 10 years to replace a whole osteon skeleton ​ Nutrition provided by intraosseous circulation Functions of bone ○​ Canals and canaliculi (cell processes of osteocytes) 1. Protection of vital organs ○​ The nutrition can spread to the next 2. Support and structure lamellae via canaliculi but spreads to 3. Movement and locomotion the next osteon via canal 4. Sound conduction ​ Characterized by slow turnover rate, higher 5. Hematopoiesis modulus of elasticity, more stiffness  LESSON 1: INTRODUCTION AND GENERALITIES 2ND SEMESTER |A.Y. 2024-2025|PROF. TRANSCRIBED BY: MAVI LAUDICO of stress -High turnover rate Elasticity Less elastic More elastic Osteon or Haversian System ​ Fundamental structural unit of a compact bone ​ Series of microscopic tubes (Haversian canals and lamellae) ​ Composed of lamellar layers; Lamellae are concentric circles and contain small opening called Cancellous (spongy or trabecular) Bone Lacunae ​ Lacuna contains osteocytes (living cell of bone) ​ 20% of total human bone ​ The lamellae is connected to another lamellae ​ Less dense through canaliculi (the lines) ​ Consists of trabeculae adjacent to irregular cavities ​ The haversian canal is the central canal and that contain red marrow contains vascular network (artery, vein, nerves) ​ Canaliculi connect to adjacent cavities that nourishes bone ​ More remodeling according to lines of stress ​ Cement layer is the last layer that determined one ​ Characterized by high turnover rate, smaller osteon to another osteon modulus of elasticity, more elasticity ​ Common in areas that experience compressive loads (ex. vertebra) CORTICAL BONE CANCELLOUS BONE Also called Compact Spongy or trabecular Found Dense portion close to Deeper structure of surface bone, with spicules forming Bone interconnecting cavity ​ 3 shapes of bones: Characteristic -Slow turnover rate -Less dense; ○​ Flat (ex. Scapula, skull) s morphology -Made of Haversian spicules that ○​ Cuboidal (ex. vertebra) system interconnect with -Bones are arranged in each other and forms ○​ Long (ex. femur, tibia) lamellar pattern spaces and contains ​ Flat and cuboidal bone consists of inner and outer marrow plate of compact bone, with cancellous bone in -Remodels between according to lines ​ Long bone:  LESSON 1: INTRODUCTION AND GENERALITIES 2ND SEMESTER |A.Y. 2024-2025|PROF. TRANSCRIBED BY: MAVI LAUDICO ○​ Medullary canal - innermost part of the bone ○​ Endosteum ○​ Cortex or shaft: composed of compact bone with haversian system ○​ Periosteum: outer fibrous covering ○​ The two ends of long bones is called epiphysis, after that is the metaphysis, the metaphysis connects the epiphysis to diaphysis ○​ Diaphysis is the shaft itself WOVEN BONE LAMELLAR BONE Immature Mature Collagen fibers intertwined Collagen fibers orderly arranged Interfibrillar spaces more Interfibrillar spaces less Formation and Formation and mineralization is faster mineralization is slower Bone Gross Anatomy Mineral density lower, Mineral density is higher, water content higher water content is lower At the ends of the long bones: 1.​ Metaphysis Mineralization matrix Mineralization collagen 2.​ Epiphysis vesicles play a role mediated ​ Both mainly made up of cancellous bone covered with thin cortex of compact bone Osteoclast can remove Osteoclast can remove ​ Epiphyseal plate (growth plate) separates woven bones totally (to be portions of lamellar bone at metaphysis and epiphysis in children; This is replaced by lamellar) a time where the cells form that’s why the bone lengthens ​ In adults, there is a line called Physis (inactive Bone according to embryonic development growth line) which means that the growth of the bone already stopped ​ Derived from mesenchyme or primitive connective tissue Bone according to pattern of collagen ​ Passes 2 process of development ○​ Membranous Lamellar ○​ Cartilaginous ​ Secondary bone Membranous bone formation ​ Fine, regular, parallel alignment of collagen, in ​ Occurs during embryonic life alternating layers called lamellae ​ Ex. Cranial vault and bones of face ​ Stronger ​ Bone already from birth ​ Predominant bone tissue in adult skeleton Cartilaginous or enchondral type of development Woven ​ Hyaline cartilage are formed in mesenchyme ​ Also called primary bone; a complex pattern of during embryonic stage interconnected elements ​ Later cartilage is invaded by blood vessels and ​ Less strong, can be laid down quickly during cartilage cells are destroyed and replaced by bone development, repair or pathologic situations ​ Long bones, spine, scapula, rib, sternum, pelvis ​ Temporary and is soon replaced by lamellar bone ​ Cartilage first then becomes bone ​ Usually found in immature bones or diseased bones  LESSON 1: INTRODUCTION AND GENERALITIES 2ND SEMESTER |A.Y. 2024-2025|PROF. TRANSCRIBED BY: MAVI LAUDICO Osteoprogenitor cells ​ Hematopoietic cells: cells where the blood vessels ​ Originate from mesenchymal cells come from; one cell that comes from this is the ​ Become osteoblasts under conditions of low strain osteoclast and increased oxygen tension ​ Mesenchymal cells: the original stem cell; from ​ Become cartilage under conditions of intermediate mesenchymal comes your bone cells, cartilage cell, strain and low oxygen tension etc. ​ Become fibrous tissue under conditions of high ​ Osteoprogenitor cells: play an important role in strain bone repair and growth ​ Line Haversian canals, endosteum and periosteum ○​ Are precursors to specialized bone cells involved in forming bone remodelling Osteoblasts compartments ​ Osteoblasts: synthesize and secrete osteoids ​ Form bone by generating organic, non-mineralized ○​ Regulate bone mineralization matrix ○​ Involved in hormone production (e.g. ​ Builds cell prostaglandins) ​ Derived from undifferentiated mesenchymal stem ○​ Form new bones cells ​ Osteocytes: make up 90-95% of all bone cells ​ Differentiation affected by interleukins, PDGF, IDGF ○​ Form from osteoblasts ○​ Involved in mechanosensation (i.e. Osteocytes detecting mechanical loading) and bone matrix maintenance and renewal ​ Maintain bone ○​ Living cells ​ Constitute 90% of the cells in the mature skeleton ​ Osteoclasts: large multinucleated bone-resorbing ​ Former osteoblasts surrounded by newly formed ○​ Two cytokines essential for osteoclast matric formation are RANK-ligand (RANKL) and ​ Less active in matrix production macrophage CSF ​ Important for control of extracellular calcium and ○​ Eat up old bones phosphorus ​ Came from osteoblasts * From bone marrow, we call it mesenchyme, from ​ Responsible for calcium control mesenchyme there is epithelial cells which becomes the skin, there are also neurons which becomes nerve cells, Osteoclasts there is also formation of cells that form muscle, lungs, and this is also where your cartilages, fats, and bone cells come ​ Resorb/Consume bone from ​ Multinucleated, irregular giant cells ​ Derived from hematopoietic cells in macrophage lineage ​ Has a ruffled brush border consisting of plasma membrane enfoldings that increase surface area for resorption ​ Bone resorption occurs in depressions (Howship's lacunae) OSTEOBLAST OSTEOCLASTS Origin From mesenchymal Macrophage-mono (stem) cell; called cyte line (from osteoprogenitor cell blood cell) Phagocytic cells Morphology Uninucleated Multinucleated Function Synthesize osteoid, Bone resorption mediates mineralization Location Lined along bone Howship’s lacunae surfaces  LESSON 1: INTRODUCTION AND GENERALITIES 2ND SEMESTER |A.Y. 2024-2025|PROF. TRANSCRIBED BY: MAVI LAUDICO calcium from kidney Bone Remodelling Cycle (decrease in absorption of phosphate) - Stimulate conversion of 25 dihydroxyvitamin D3 to 1,25 dihydroxyvitamin D3 which increases intestinal absorption of calcium ​ Bone remodelling stars with the Quiet Phase. Now, when our bones are subject to stress (for ex. Our Calcitonin - Inhibits production and - Bone formation Femur when walking), it gets degenerated over activity of osteoclast and decrease osteoclastic bone time. It will now call your osteoclasts to come in resorption (Recruitment phase). Once the osteoclasts eat up the old bone, it will erode (Resorption phase). Thyroid - Increase osteoblast - Bone formation, Once it is eaten up, osteoblast will come in stimulating differentiation prevention of bone (Reversal phase). Osteoblast will build a new bone hormone loss (Formation). After the bone was formed, it will now - Decrease osteoclast go under Mineralization, and then back to Quiet formation and survival Phase again. Cortisol - Decrease maturation, - Bone loss ​ If the bone is continuously eaten up and is slow in lifespan and function of remodeling, the bone will not be rebuild properly osteoblast and will become fragile through time. ​ Everytime a cell is destroyed, the calcium that is Estradiol - Increase osteoblast - Bone formation, inside the cell goes out. It will go back to the blood proliferation and prevention of bone and it will now function to other parts of the body differentiation loss - Decrease osteoclast differentiation ​ The younger the person is, the more active the remodeling. As the person goes older, it gets slower Testosterone - Increased osteoblast - Bone formation, ​ When there is more stress to the bone, the faster proliferation and prevention of bone the turnover. That is why the bone is always new. differentiation loss ○​ Also the reason why old people are encouraged to move FST - Increase osteoblast - Bone formation, (follistatin) proliferation prevention of bone ○​ As a person gets older, the replacement of loss bone also gets slower Hormone Action Role PTH - Increase osteoclast - Bone formation (Parathyroid) proliferation - Bone loss Estrogen - Modulates resorption of - Bone formation (more trabecular bone through - Menopausal - Increase osteoblast dominant in activation of estrogen women are more proliferation (in small females) receptors on bone cell prone to amounts) osteoporosis - Prolongs osteoblastic life Vitamin D - Increase osteoblast - Bone formation, span, shorten osteoclastic differentiation prevents bone life span loss - Indirectly suppresses IGFI (insulin - Increase osteoblast - Bone formation, cytokines (e.g. interleukin 6) like growth proliferation and prevents bone that stimulates bone factor) differentiation loss resorption Parathyroid - Regulate blood calcium - Bone hormone resorption/loss - Low calcium, PTH release calcium from bone (indirect stimulation of bone resorption or osteoclast), and enhance absorption of  LESSON 1: INTRODUCTION AND GENERALITIES 2ND SEMESTER |A.Y. 2024-2025|PROF. TRANSCRIBED BY: MAVI LAUDICO ​This system arises from the periarticular vascular plexus (e.g. Bone Matrix geniculate arteries) ​ Not exactly from the main artery ​ Organic components: 40% of dry weight of bone ○​ Periosteal system ○​ Collagen (90%) ​ Consists mostly of capillaries that ​ Primarily collagen type 1 supply the outer third of the ​ Provides tensile strength mature diaphyseal cortex ○​ Proteoglycans ​ Small capillaries that penetrate ​ Partly responsible for the bone compressive strength ​ Blood pressure in this system is ○​ Matrix proteins low ​ Promote mineralization and bone Direction of Blood Flow formation ​ Osteocalcin, osteonectin ​ Arterial flow in mature bone centrifugal (inside to ○​ Growth factors and cytokines outside) due to the net effect of the high-pressure ​ Inorganic components: 60% of dry weight of bone nutrient artery system and the low-pressure ○​ Calcium Hydroxyapatite periosteal system ​ Ca10(PO4)6(OH)2 ○​ The nutrient artery goes to the central ​ Provides compressive strength canal of the Haverian system. Once it ○​ Calcium phosphate reaches the canal, the pressure is high as it flows outside ​ In fractures and in immature, developing bone, Bone Remodeling blood flow is centripetal (outside to inside) because the nutrient artery system is disrupted ​ Cortical and cancellous bone are continuously ​ Venous flow in mature bone is centripetal (cortical remodeled throughout life by osteoblastic and capillaries drain to venous sinusoids which drain to osteoclastic activity the emissary venous system) ​ Wolff’s law: remodeling occurs in response to mechanical stress ○​ The more you put stress, the faster the Tissues surrounding the bone remodeling ​ Hueter-Volkmann Law: compressive forces inhibits Periosteum growth; tension stimulates it ​ Connective tissue membrane which covers the ○​ Ex. If you have a child patient with bone scoliosis, the compressive force inhibits ​ Highly developed in children the development or remodeling of the bone ​ Parts: but the tensed area or the stretched are ○​ Cambium layer has faster remodeling, thus it grows ​ Inner periosteum abnormally ​ Loose and vascular ​ Contains cells capable of becoming osteoblasts which Bone Circulation enlarge the diameter of bone during growth and form periosteal ​ Bone receives 5-10% of the cardiac output callus during fracture healing ​ Long bones receive blood from 3 systems: ○​ Fibrous layer ○​ Nutrient artery system ​ Outer periosteum ​ Branch from systemic arteries, ​ Less cellular and continuous with enter the diaphyseal cortex joint capsules through the nutrient foramen, enter the medullary canal and branch into ascending and descending arteries ​ Blood pressure in this system is high because it came from the main artery ○​ Metaphyseal-epiphyseal system  LESSON 1: INTRODUCTION AND GENERALITIES 2ND SEMESTER |A.Y. 2024-2025|PROF. TRANSCRIBED BY: MAVI LAUDICO * Cleidocranial dysostosis is a problem with intramembranous development, which can happen as deformities in the skull or face * Paget’s disease occur in appositional development wherein there is a fast osteoclastic activity which therefore eats up the bone before it is completely rebuilt, resulting to weaker and more fragile bone formation Enchondral Ossification ​ Epiphyseal plate - growth plate ○​ Mostly enchondral ossification happens ○​ Growth spurt of children affected by growth hormones and puberty Bone Marrow ○​ Zone of cartilage that forms between ​ Source of progenitor cells diaphysis and epiphysis ​ Found inside the medullary cavity of the long bone ○​ Enchondral ossification – complex process ​ Types: ○​ Zones: ○​ Red Marrow Zone of Reserve Made of hyaline cartilage ​ Hematopoietic Cartilage and chondrocytes ​ 40% water, 40% fat, 20% protein ​ Slowly changes to yellow marrow Zone of proliferation Chondrocytes divide with age rapidly and form parallel ○​ Yellow Marrow columns ​ Inactive Zone of maturation Chondrocytes stop dividing ​ 15% water, 80% fat, 5% protein and begin to enlarge Zone of hypertrophy and Cell enlarge; Starts to calcification calcify (calcium mineralization Zone of cartilage Most chondrocytes (close degeneration to diaphysis) are dead because the matrix around them has calcified Zone of osteogenesis Formation of bone (blood supply, etc.) Physis ​ Growth plates in immature long bones ​ Physeal cartilage zones: ○​ Reserve zone ○​ Proliferative zone ○​ Hypertrophic zone ​ Maturation zone ​ Degenerative zone ​ Zone of provisional calcification * Enchondral came from cartilage first before becoming a bone; Intramembranous is already a bone from birth; If the enchondral is disrupted, the bone growth will be halted resulting to shorter bone compared to its normal counterpart (Achondroplasia)  LESSON 1: INTRODUCTION AND GENERALITIES 2ND SEMESTER |A.Y. 2024-2025|PROF. TRANSCRIBED BY: MAVI LAUDICO ​ Low oxygen tension and decreased proteoglycans aggregates ​ Example disease: rickets(lack of vitamin D) (zone of provisional calcification), mucopolysaccharide diseases (zone of maturation and degeneration) 1. Congenital anomalies: abnormalities in the development of the limbs and spine Reserve Zone ​ Genetic abnormalities ​ Environmental changes affecting the developing ​ Where the chondrocytes are fetus ​ Cells store lipids, glycogen and proteoglycans ​ Combination ​ Decreased oxygen tension ​ Example disease: Lysosomal storage diseases (e.g. Gaucher’s disease) Proliferative Zone ​ Growth is longitudinal 2. Trauma ​ Stacking of chondrocytes ​ Mechanical injury (acute or chronic) causing sprain, ​ Cellular proliferation and matrix production fracture, degenerative disc disease ​ Increased oxygen tension and increased proteoglycans inhibit calcification ​ Growth hormone exerts its effect in this zone ​ Example disease: Gigantism (if growth hormones are too much), Achondroplasia (if growth hormones are inactive) 3. Infection: ​ Pathogenic organisms enter bone (osteomyelitis or joint septic arthritis) Hypertrophic Zone ​ Blood stream ​ Directly from open wounds or ​ Divided into 3 zone: maturation, degeneration ​ Extension from a neighboring focus and provisional calcification ​ Normal matrix mineralization ​ Chondrocytes increase 5x in size, accumulate calcium in mitochondria, die, and release calcium for matrix vesicles ​ Osteoblasts migrate from sinusoidal vessels and use cartilage as a scaffolding for bone formation  LESSON 1: INTRODUCTION AND GENERALITIES 2ND SEMESTER |A.Y. 2024-2025|PROF. TRANSCRIBED BY: MAVI LAUDICO 4. Metabolic disorders: ​ Metabolic disturbances causing changes in and about the bones and joints Diagnosis ​ E.g. Gouty arthritis-disturbance of purine metabolism History taking 1.​ Basic information (age, sex, occupation, racial background, economic status 2.​ Chief complaint a.​ Pain (location, severity, description, pain scale, time, relieving and aggravating factors) 5. Endocrine disorders: 3.​ Time and manner of onset ​ Extensive changes in the bone due to abnormalities 4.​ History of present illness of the endocrine gland 5.​ Review of system ​ Eg. bone resorption with hyperparathyroidism Physical Examination 1. Inspection 2. Palpation 3. Range of motion -​ Goniometer 6. Tumors: 4. Special tests ​ Abnormal growths in the bone 5. Neurologic examination ​ Benign (more amenable to treatment) or malignant (more serious prognosis) Diagnostic Procedures Physical examination 1. Laboratory 2. Ancillary procedures -​ Radiologic findings -​ Xray, CTscan, MRI -​ Musculoskeletal Ultrasound -​ EMG-NCV tests 7. Circulatory disorders: Management ​ Disturbances in blood supply (esp in the physis) causes changes in growth due to lack of nutrients Rehabilitation Medicine ​ Lesions are called aseptic, ischemic or ​ Program are designed to osteonecrosis ○​ Restore patient to maximum functional ​ Disturbances that increase blood flow to an activity as early as possible epiphysis (e.g. healing fracture) may increase bone ○​ Facilitate patient’s adjustment and length adaptation to work, home and community 8. Neurologic disorders: ○​ Help patient know how to compensate to ​ Lesions in the brain: Cerebral palsy their impairment/disability ​ Lesions in the spinal cord: paraplegia, poliomyelitis ​ Lesions in the peripheral nerve: localized paralysis 9. Psychological disorders: ​ Psychiatric disorders may lead to joint lesions (contractures)